Báo cáo y học: " Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài: " Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells. | Kim et al. Respiratory Research 2011 12 49 http content 12 1 49 RESPIRATORY RESEARCH RESEARCH Open Access Cigarette smoke exacerbates mouse allergic asthma through Smad proteins expressed in mast cells Dae Yong Kim1t Eun Young Kwon1t Gwan Ui Hong1 Yun Song Lee1 Seung-Hyo Lee2 and Jai Youl Ro1 Abstract Background Many studies have found that smoking reduces lung function but the relationship between cigarette smoke and allergic asthma has not been clearly elucidated particularly the role of mast cells. This study aimed to investigate the effects of smoke exposure on allergic asthma and its association with mast cells. Methods BALB c mice were sensitized and challenged by OVA to induce asthma and bone marrow-derived mast cells BMMCs were stimulated with antigen antibody reaction. Mice or BMMCs were exposed to cigarette smoke or CSE solution for 1 mo or 6 h respectively. The recruitment of inflammatory cells into BAL fluid or lung tissues was determined by Diff-Quik or H E staining collagen deposition by Sircol assay penh values by a whole-body plethysmography co-localization of tryptase and Smad3 by immunohistochemistry IgE and TGF-p level by ELISA expressions of Smads proteins activities of signaling molecules or TGF-p mRNA by immunoblotting and RT-PCR. Results Cigarette smoke enhanced OVA-specific IgE levels penh values recruitment of inflammatory cells including mast cells expressions of smad family TGF-p mRNA and proteins and cytokines phosphorylations of Smad2 and 3 and MAP kinases co-localization of tryptase and Smad3 and collagen deposition more than those of BAL cells and lung tissues of OVA-induced allergic mice. CSE solution pretreatment enhanced expressions of TGF-p Smad3 activities of MAP kinases NF-kB AP-1 or PAI-1 more than those of activated-BMMCs. Conclusions The data suggest that smoke exposure enhances antigen-induced mast cell activation via TGF-p Smad signaling pathways in mouse allergic asthma and that it exacerbates .

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